Role of peripheral vasodilation in the hypotensive response to left ventriculography in anesthetized dogs

Abstract

Hypotension after left ventriculography (LVG) is believed to result from direct myocardial toxicity, peripheral vasodilation, or a combination of both. The contribution of each has not been established. Thus, LVG was performed in anesthetized dogs under conditions in which peripheral vascular reactivity (PVR) was altered pathophysiologically (aortic coarctation) or pharmacologically (acetylcholine infusion). Ventricular pressure (LVP), its first derivative (dP/dt), aortic pressure (A(o)P), and carotid and femoral flows were monitored. When PVR was normal, LVG was associated with significant hemodynamic changes which reached a maximum 25-35 seconds after injection. Left ventricular and aortic diastolic pressures were decreased by 22 and 48%, whereas carotid and femoral systolic flows were increased by 41 and 59%. During acetylcholine infusion, LVG did not cause systolic hypotension and peripheral flows were maintained strikingly constant. Similarly, LVG also was associated with insignificant changes in systolic pressures and carotid flow in the presence of aortic coarctation. These results demonstrate that the hypotension attendant with LVG is directly related to the augmentation in peripheral flow, suggesting that the response is mediated almost exclusively by peripheral vasodilation.